ArticleBritish journal of pharmacology2003
Substance P modulates localized calcium transients and membrane current responses in murine colonic myocytes.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 22 citations in OpenAlex.
- Contractile effect of tachykinins on rabbit small intestine.Acta pharmacologica Sinica · 2011Article
- Tachykinin NK2 receptor antagonists for the treatment of irritable bowel syndrome.British journal of pharmacology · 2004Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. Neurokinins contribute to the neural regulation of gastrointestinal (GI) smooth muscles. We studied responses of murine colonic smooth muscle cells to substance P (SP) and NK(1) and NK(2) agonists using confocal microscopy and the patch clamp technique. 2. Colonic myocytes generated localized Ca(2+) transients that were coupled to spontaneous transient outward currents (STOCs). SP (10(-10) M) increased Ca(2+) transients and STOCs. Higher concentrations of SP (10(-6) M) increased basal Ca(2+) and inhibited Ca(2+) transients and STOCs. 3. Effects of SP were due to increased Ca(2+) entry via L-type Ca(2+) channels, and were mediated by protein kinase C (PKC). Nifedipine (10(-6) M) and the PKC inhibitor, GF 109203X (10(-6) M) reduced L-type Ca(2+) current and blocked the effects of SP. 4. SP responses depended upon parallel stimulation of NK(1) and NK(2) receptors. NK(1) agonist ([Sar(9),Met(O(2))(11)]-substance P; SSP) and NK(2) agonists (neurokinin A (NKA) or GR-64349) did not mimic the effects of SP alone, but NK(1) and NK(2) agonists were effective when added in combination (10(-10)-10(-6) M). Consistent with this, either an NK(1)-specific antagonist (GR-82334; 10(-7) M) or an NK(2)-specific antagonist (MEN 10,627; 10(-7) M) blocked responses to SP (10(-6) M). 5. Ryanodine (10(-5) M) blocked the increase in Ca(2+) transients and STOCs in response to SP (10(-10) M). 6. Our findings show that low concentrations of SP, via PKC-dependent enhancement of L-type Ca(2+) current and recruitment of ryanodine receptors, stimulate Ca(2+) transients. At higher concentrations of SP (10(-6) M), basal Ca(2+) increases and spontaneous Ca(2+) transients and STOCs are inhibited.
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